1 Adrenergic receptor and G s mRNAs in rat heart as a function of mechanical load and thyroxine intoxication

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Abstract
Objective: The aim of this study was to determine the expression of genes coding for the β1 adrenergic receptor and the α subunit of Gs in the adult rat normal and hypertrophied left ventricle, and in the left ventricle of the hypophysectomised rat after T4 intoxication. Methods: Total RNA was extracted from normal, control, or hypertrophied left ventricles 5 weeks after aortic stenosis, and from left ventricles of control or T4 injected hypophysectomised animals. The expression of β1 adrenergic receptor and Gαas mRNAs was quantitated by northern blot analysis and hybridisation with specific 32P-dCTP labelled DNA probes. Results: β1 Adrenergic receptor mRNA was decreased (by 33%) in compensated left ventricular hypertrophy without modification of the relative level of Gαs mRNA. The relative level of β1 adrenergic receptor mRNA correlated negatively with the degree of left ventricular hypertrophy, suggesting that the expression of the β1 adrenergic receptor gene is not activated by pressure overload. In the left ventricle of the hypophysectomised rat, a rapid increase in β1 adrenergic receptor mRNA (by 180% 3 h after hormone injection) was observed in response to T4, with no change in the relative content of Gαs mRNA. These results provide evidence that β1 adrenergic receptor mRNA and Gas mRNA accumulate to different levels of abundance in the adult left ventricle, as indicated by their ratios (0.053 and 0.043 in sham operated and hypertrophied left ventricles respectively). This suggests that distinct mechanisms are involved in the control of the accumulation of these two mRNAs in cardiac tissue. Conclusions: The reduction in β1 adrenergic receptor density in the hypertrophied rat left ventricle is associated with a parallel reduction in the level of β1 adrenergic receptor mRNA. The β1 adrenergic receptor gene may belong to a group of genes which are not activated by pressure overload, but are responsive to thyroid hormone. Cardiovascular Research 1993;27:231-237

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